Search

Nanoplastics, an emerging contaminant, pose risks to fetal neural development, transferring from mother to offspring via placenta and breast milk. Assessing these risks, hippocampal CA3 samples from nanopolystyrene-exposed rat offspring were proteomically analyzed. Findings revealed reduced expression of neural developmental proteins (KIF21A, STMN2, DMTN, DLG1) and increased inhibitory proteins (PZP, α-2M, FN1, SERPINA1, ALOX15) in the hippocampus. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis highlighted ferroptosis enrichment, validated by significantly expressed ALOX15 and TF proteins. These alterations suggest nanopolystyrene's potential contribution to cognitive deficits and neurodevelopmental disorders, emphasizing its hazardous impact on neural development. This study provides novel insights into nanopolystyrene's risks. [ABSTRACT FROM AUTHOR]

Objective: This study was designed to investigate the risk factors of postoperative acute kidney injury (AKI) in patients with complex congenital heart disease (CHD) and the significance of early detection of serum transcription factor Nkx2.5., Methods: A total of 121 CHD patients admitted to the Shengli Clinical Medical College of Fujian Medical University were selected as study participants, among whom 69 patients with AKI after cardiac surgery were set as the research group (RG), and the rest of the 52 patients without AKI were set as the control group (CG). Cardiopulmonary bypass (CPB) duration, aortic occlusion time, postoperative creatinine (Cr) level and mechanical ventilation (MV) time were compared between the two groups. The expression and clinical significance of Nkx2.5 in the two groups were detected. Intensive Care Unit (ICU) residence time and total hospital stay were compared, and the risk factors were analyzed., Results: The RG presented remarkably longer CPB duration and aortic occlusion time, evidently higher postoperative Cr level and longer MV time, and observably lower Nkx2.5 level in comparison to the CG (all P<0.05). According to the analysis of receiver operating characteristic (ROC) curves, Nkx2.5 displayed a favorable diagnostic value in predicting the occurrence of CHD complicated with AKI. ICU residence time and total hospital stay were longer in the RG than in the CG (P<0.05). CPB time and aortic occlusion time were independent risk factors for AKI in CHD patients, while surgical methods and Nkx2.5 detection were independent protective factors (P<0.05)., Conclusions: CPB time, aortic occlusion time and surgical methods, as well as Nkx2.5 detection are independent factors affecting AKI in patients with CHD. Early detection of serum transcription factor Nkx2.5 is of particular importance for clinical diagnosis of CHD patients complicated with AKI., Competing Interests: None., (AJTR Copyright © 2021.)

Objective: To investigate the impairment of lead exposure on rat hypothalamus and striatum., Methods: Forty-five healthy SPF male SD rats were randomly divided into three groups, control group( double distilled water), low( 60 mg/kg BW) and high dose( 120 mg/kg BW) groups. The rats were treated with lead acelate water solution in lead exposure group by gavage for 9 weeks. Open-field test was used to detect behavioral changes of the rats. The lead content of hypothalamus and striatum was determined by inductively coupled plasma mass spectrometry( ICP-MS). The mRNA expressions of toll-like receptor 4( TLR4), nuclear transcription factor kappa B( NF-κB), tumor necrosis factors alpha( TNF-α), interleukin-1( IL-1β) and 8-oxoguanine DNA glycosylase( OGG1) were measured by real-time PCR. Enzyme linked immunosorbent assay( ELISA) was applied to detect the protein content of TLR4, NF-κB, TNF-α, IL-1β and 8-hydroxy-2-deoxyguanosine( 8-OHd G)., Results: There were no significant differences in terms of body weight among three groups of rats. Compared with the control group, total movement distance, the total number of lattice and the distance of the central region in low and high lead exposure group were significantly decreased( P < 0. 05). The lead contents in hypothalamus and striatum of rats of low and high lead exposure group were( 60. 10 ± 6. 71), ( 71. 20 ± 11. 24), ( 44. 07 ± 9. 63)and( 66. 67 ± 8. 78) μg/g, respectively, higher than those in the control group(( 33. 77± 8. 19), ( 25. 75 ± 6. 33) μg/g)( P < 0. 05). While compared with the control group, the mRNA expression of NF-κB and OGG1 of the low and high lead exposure group were( 3. 47 ± 0. 15), ( 1. 43 ± 0. 16) and( 0. 67 ± 0. 13), ( 0. 57 ± 0. 19) folds in hypothalamus, there were marked differences in the mRNA expression of TLR4 and NF-κB between low and high lead group. The NF-κB, TNF-α, IL-1β protein contents in hypothalamus of the low lead exposure group were( 5. 85 ± 1. 10), ( 56. 15 ± 6. 96) and( 1. 18 ± 0. 20) ng/g, respectively higher than those in control group(( 3. 03 ± 0. 71), ( 49. 25 ± 7. 21) and( 0. 86 ± 0. 11) ng/g)( P < 0. 05). The TLR4, NF-κB, TNF-α, IL-1β protein contents in hypothalamus of the high lead exposure group were( 0. 67 ± 0. 12), ( 4. 74 ± 0. 68), ( 69. 73 ± 9. 61) and( 1. 43 ± 0. 29) ng/g, respectively, higher than those in control group. There were marked differences in the protein contents of TLR4 and TNF-α significant between low and high lead group in hypothalamus. The mRNA expression of TLR4, NF-κB, IL-1β in the striatum of rats in the high lead exposure group were significantly higher than those in control group( P < 0. 05). The TLR4, NF-κB, TNF-α, IL-1β, 8-OHd G protein contents of the high lead exposure group were( 0. 33 ±0. 02) ng/g, ( 4. 66 ± 0. 51), ( 82. 63 ± 7. 99), ( 1. 92 ± 0. 35) and( 1. 21 ± 0. 14) ng/g, respectively higher than those in control group( P < 0. 05), NF-κB protein content of the high lead exposure group was higher than that in low lead exposure group( P < 0. 05)., Conclusion: Lead exposure does result in the impairment of hypothalamus and striatum, indicating that inflammation and oxidative damage might be involved in this process.

Objective: To investigate the effects of lead exposure on the copper concentration in the brain and serum and the expression of copper transporters in the choroid plexus among rats., Methods: Sixty specific pathogen-free Sprague-Dawley rats were randomly divided into a control group and three lead-exposed groups, with 8 mice in each group. The lead-exposed groups were orally administrated with 500 (low-dose group)), 1 000 (middle-dose group), and 2 000 mg/L (high-dose group) lead acetate in drinking water for eight weeks. And the rats in control group were given 2 000 mg/L sodium acetate in drinking water. The content of lead and copper in the serum, hippocampus, cortex, choroid plexus, bones, and cerebrospinal fluid (CSF) was determined by inductively coupled plasma-mass spectrometry (ICP-MS). Confocal and real-time PCR methods were applied to measure the expression of copper transporters including copper transporter 1 (Ctr1), antioxidant protein 1 (ATX1), and Cu ATPase (ATP7A)., Results: Compared with the control group, the lead-exposed groups showed significantly higher lead concentrations in the serum, cortex, hippocampus, choroid plexus, CSF, and bones (P < 0.05) and significantly higher copper concentrations in the CSF, choroid plexus, serum, and hippocampus (P < 0.05). Confocal images showed that Ctr1 protein was expressed in the cytoplasm and cell membrane of choroid plexus in control group. However, Ctr1 migrated to CSF surface microvilli after lead exposure. Ctr1 fluorescence intensity gradually increased with increasing dose of lead, except that the middle-dose group had a higher Ctr1 fluorescence intensity than the high-dose group. In addition, the middle- and high-dose groups showed a lower ATX1 fluorescence intensity compared with the control group. Real-time PCR data indicated that the three lead-exposed groups showed significantly higher mRNA levels of Ctr1 and ATP7A compared with the control group (P < 0.05)., Conclusion: Copper homeostasis in the choroid plexus is affected by lead exposure to induce copper homeostasis disorders in brain tissue, which may be one of the mechanisms of lead neurotoxicity.